The goal of this research project is to determine the mechanism whereby patients with severe chronic alcoholism develop phosphorus deficiency and in turn, how phosphorus deficiency is related to the development of alchoholic myopathy which occurs so commonly in such patients. Thus far, we have established that experimental phosphorus deficiency in the dog induces injury to the skeletal muscle cell as reflected by abnormal sodium and potassium transport activity as well as depression of the resting electrical transmembrane potential. Using an experimental model which closely resembles that seen in a number of patients with chronic alcoholism and malnutrition, namely, underfeeding in conjunction with phsophorus deficiency, induction of severe hypophosphatemia by hyperalimentation converts the electrochemical myopathy into overt necrosis of skeletal muscle and at least in some instances, simultaneous myoglobinuria. Our studies to date have also mimicked the well-established clinical observation on alcholic patients that acute starvation of several days duration superimposed upon the chronic alcoholic state commonly is associated with rapid deterioration of skeletal muscle cells. Studies are currently underway to examine the precise effects of magnesium deficiency on muscle phosphorus content as well as content of other ions. We are also examining the effect of chronic ethanol administration on cellular sodium and potassium transport characteristics in experimental animals.